The proposed experiments will investigate the functional dissociation of the estrogenic suppression of food intake and induction of sexual receptivity. It is hypothesized that these two estrogen-induced behaviors are mediated at different neural sites. Specifically, it is hypothesized that estrogenic stimulation of the paraventricular nucleus (PVN) is sufficient to lower food intake but not affect reproductive behavior. The methodology will involve treating ovariectomized rats with varying doses of 17 beta-estradiol or 17 alpha-estradiol in different brain regions, and measuring the changes in both food intake and lordosis in the same subjects. A correlational analysis of implant location and the behavioral changes produced by hormonal stimulation will be used to determine the true site of estrogen's actions within the brain. In this way, one would be able to selectively study a population of estrogen-sensitive neurons that are primarily involved in the appetitive, but not the reproductive, effects of estradiol. Future studies would examine the interactions between estrogens, neurotransmitters, and neuropeptides that control feeding, so that the biochemical substrate for the estrogenic suppression of food intake could be more clearly elucidated. These studies have important implications for understanding the mechanisms underlying endocrine-related eating disorders such as anorexia nervosa and some forms of obesity.